ArticleMolecular and cellular biochemistry2018
MCAM knockdown impairs PPARγ expression and 3T3-L1 fibroblasts differentiation to adipocytes.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Integrated lipidomics and RNA sequencing analysis reveal novel changes during 3T3-L1 cell adipogenesis.PeerJ · 2022Article
- Alendronate inhibits triglyceride accumulation and oxidative stress in adipocytes and the inflammatory response of macrophages which are associated with adipose tissue dysfunction.Journal of physiology and biochemistry · 2021Article
- Liver Kinase B1 Fine-Tunes Lineage Commitment of Human Fetal Synovium-Derived Stem Cells.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020Article
- The Antiobesity Effects of Buginawa in 3T3-L1 Preadipocytes and in a Mouse Model of High-Fat Diet-Induced Obesity.BioMed research international · 2019Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
We investigated for the first time the expression of melanoma cell adhesion molecule (MCAM) and its involvement in the differentiation of 3T3-L1 fibroblasts to adipocytes. We found that MCAM mRNA increased subsequent to the activation of the master regulator of adipogenesis, PPARγ, and this increase was maintained in the mature adipocytes. On the other hand, MCAM knockdown impaired differentiation and induction of PPARγ as well as expression of genes activated by PPARγ. However, events that precede and are necessary for early PPARγ activation, such as C/EBPβ induction, β-catenin downregulation, and ERK activation, were not affected in the MCAM knockdown cells. In keeping with this, the increase in PPARγ mRNA that precedes MCAM induction was not altered in the knockdown cells. In conclusion, our findings suggest that MCAM is a gene upregulated and involved in maintaining PPARγ induction in the late but not in the early stages of 3T3-L1 fibroblasts adipogenesis.
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Registered trials
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